The present invention relates generally to a method and composition for preventing or reducing the symptoms of insulin resistance syndrome in a person.
An insulin resistance syndrome that has been identified as “Syndrome X” by previous research is a common metabolic disorder affecting more than 75 million Americans to some degree. Insulin resistance is a condition in which the body becomes resistant to its own insulin. The body of the person affected compensates by releasing more insulin, elevating body insulin levels. This elevated insulin level leads to increased risk of a variety of symptoms, including diabetes, obesity, and heart disease.
Syndrome X appears to be highly prevalent in the obese. Individual elements of Syndrome X (obesity, hypertension, lipid disturbances, and glucose intolerance) are frequently encountered during a typical person's life span, and they tend to be increasing apparent as people age, usually becoming most prevalent after age 35. Theoretical considerations suggest that insulin resistance may be a primary factor that plays a causative role in the induction of both obesity and diabetes. Atherogenic risk factors associated with obesity and Syndrome X contribute independently to the development of atherosclerotic disease, and risk of a cardiovascular event increases sharply with the burden of risk factors associated with obesity.
Animal models of Syndrome X, as observed in rats fed high fat diets, exhibit excess accumulation of muscle triglyceride coincident with development of insulin resistance. This also seems to occur in humans; several studies demonstrate increased muscle triglyceride content in insulin resistant states. There is substantial evidence indicating that excess muscle and liver lipid accumulation causes or exacerbates insulin resistance in Syndrome X and in Type II diabetes. Development of strategies to prevent this, therefore, seem worthwhile.
Avoiding weight gain from adolescence to middle age is known to reduce cardiovascular morbidity and mortality. Despite much debate in the past regarding the influence of obesity on health and the benefits of maintaining normal weight, it is clear that changes in weight correlate to changes in several atherogenic risk factors. Recent perspective studies indicate a continuous graded influence of body mass index (BMI), the ratio of weight expressed in kilograms divide by the height meters squared, on the rate of coronary disease development. Increased risk is evident at BMI levels below average, indicating that moderate obesity can be unhealthy. Central obesity, typically including measurements of waist girth or waist to hip ratio, has been shown to be more metabolically disadvantageous than other forms of obesity and, as a consequence, it is considered a strong predictor of cardiovascular disease.
The mechanism whereby obesity and weight gain promote atherogenic risk factors and, in turn, cardiovascular disease is well established. Excess body fat has been shown to increase resistance to insulin action and reduce uptake of glucose by peripheral tissues. Abdominal obesity, in particular, is associated with insulin resistance, hyperinsulinemia, a relative deficiency of lipoprotein lipase, elevated triglycerides, reduced HDL-cholesterol and small dense LDL-particles. Obesity may promote increased absorption in the renal tubules, expanding blood volume and inducing an autonomic imbalance that results in hypertension. In addition, insulin resistance often eventuates into glucose intolerance and diabetes which in turn accelerates atherogenesis.
Obesity is clearly the most prevalent metabolic disorder in the United States, and weight control deserves a high priority to curb cardiovascular disease and the associated predisposing conditions, such as lipidemia, hypertension and glucose intolerance. The benefits of weight control on the major atherogenic risk factors and the insulin resistance syndrome should provide a strong incentive and rationale for control of obesity. There is no other risk factor that affects the cardiovascular risk profile as strongly. It is well known that non-insulin dependent type II diabetes is highly associated with obesity. It has been reported that healthy persons with elevated insulin levels have increased levels of LDL cholesterol, decreased HDL cholesterol and high blood pressure compared with healthy individuals who have normal insulin levels. Diabetes is associated with high blood lipids, hypertension and a tendency of blood platelets to clot, which can block arteries resulting in heart attack or stroke. Diabetes causes a defect in glucose homeostasis. Weight control is a logical first approach to avoid moderate degrees of hypertension, dyslipidemia, glucose tolerance and hyperinsulinemia that constitute Syndrome X.
To overcome glucose tolerance, patients with syndrome X secrete large amounts of insulin. Treatment of Syndrome X should therefore be aimed at: 1) increasing insulin sensitivity; 2) attenuating day-long hyperinsulinemia; and 3) pharmacologic treatment of the specific manifestations of syndrome X, if lifestyle interventions such as weight loss are not entirely successful. The two major lifestyle modulators of insulin action are body weight and physical fitness; the heavier and the more sedentary a patient is, the greater the degree of insulin resistance and compensatory hyperinsulinemia.
However, even with control of weight, many people can still develop Syndrome X. Also, many people find controlling their weight to be difficult, and they are unsuccessful in their attempts. Therefore, pharmacological treatments are needed to help reduce the effects of Syndrome X in persons.
Chromium helps insulin metabolize fat, turn protein into muscle and convert sugar into energy. It is an essential trace element required for normal protein, fat and carbohydrate metabolism. Chromium levels are known to decrease with age, and marginal chromium deficiencies appear to be widespread. Chromium is important for energy production and plays a role in regulating appetite, reducing sugar cravings, and increasing lean body mass.
Niacin-bound chromium (also called chromium nicotinate or chromium polynicotinate) dramatically increases the effectiveness of chromium in a person ingesting it. Normally, chromium is poorly absorbed and utilized by the body. However, researchers have found that the most potent form of chromium in nature is that form bound to the B-vitamin, niacin. Furthermore, previous research discoveries led to the identification of Glucose Tolerance Factor or “GTF”, a biologically active form of chromium that facilitates normal insulin function, which is responsible for normal glucose (blood sugar) metabolism. Researchers have found that a particular oxygen-coordinated chromium niacin complex is the most potent form of all, being over eighteen times more potent than the next closest form of niacin-bound chromium tested.
In 1997, researchers at the University of Tex., Austin, showed that a combination of administration of niacin-bound chromium along with exercise in obese women resulted in a significant weight loss in the women and also lowered the increase in insulin levels when the women were orally fed glucose. In contrast, those taking chromium picolinate, a different form of chromium, were found to show significant weight gain. In 1999, researchers at Georgetown University Medical Center showed that compared to a placebo, niacin-bound chromium caused significant loss of body fat and sparing of muscle (lean body mass) in overweight African-American women. Also, tests on the blood chemistries of the women revealed no significant adverse effects from the ingestion of 600 μg of elemental chromium daily for 2 months. This observation demonstrated the safety of administration of niacin-bound chromium at the tested levels.
In 1994, researchers at Auburn University showed that supplementation with 200 mcgs of niacin-bound chromium significantly lowered moderate levels of cholesterol by an average of 14 percent and improved the ratio of total cholesterol to HDL (“good”) cholesterol by 7 percent in male athletes. In 1995, researchers at Georgetown University Medical Center showed that a combination of niacin-bound chromium and soluble fiber (i.e., guar) significantly inhibited sugar-induced high blood pressure in rats. In 1997, researchers at Georgetown University Medical Center showed that niacin-bound chromium inhibited sugar-induced high blood pressure, improved long-term blood sugar status and reduced liver and kidney lipid peroxidation in rats. In 2000, researchers at Georgetown University Medical Center showed that a combination of niacin-bound chromium and grape seed proanthocyanidin extract significantly lowered both total cholesterol levels and LDL (“bad”) cholesterol levels by 10 and 14 percent, respectively, in people with elevated blood cholesterol levels.
Diabetic patients have been found to have lower serum chromium levels and a higher chromium excretion rate. Treatment with niacin-bound chromium has been found to improve glucose tolerance in diabetic patients. Dietary trivalent chromium has been shown to have significant beneficial effects on the insulin system.
It has been demonstrated that essential hypertension may be due to insulin perturbations. As high dose chromium supplementation seems nontoxic, chromium may prove to be a useful means to lower blood pressure in some essential hypertensives as well as diabetic hypertensives. It also has been shown that chromium supplementation may prove to be the most useful means to prevent or treat type II diabetes mellitus and related cardiovascular disorders. Chromium supplementation amplifies insulin receptor tyrosine kinase activity, which explains the relationship between chromium and its effects in diabetes. Chromium further reduces vascular smooth muscle calcium loads and thus reduces peripheral vascular resistance in insulin-resistant states.
Recently, the U.S. Department of Agriculture (USDA) found that many middle-age diabetics could overcome their symptoms by taking a chromium supplement. The USDA's findings suggest that very low chromium intakes may be putting millions of Americans on the road to diabetes (and high blood cholesterol) and that the process could be reversed by supplementing with chromium. A separate study found that marginal chromium loss in male athletes resulting in impaired insulin function can be improved by supplementation with niacin-bound chromium.
However, though the above studies demonstrate that administering niacin-bound chromium may serve as a beneficial therapeutic method for reducing or preventing the various symptoms associated with Syndrome X, this has not been entirely effective. Improved methods and compositions, therefore, are necessary to provide for preventing or and reducing the symptoms of Syndrome X in persons. The present invention fulfills this need and provides for further advantages.